A study has suggested that hypertension-induced sodium excretion via eNOS- and COX-2 (cyclooxygenase-2)-dependent pathways in kidneys is facilitated by the absence of lymphocyte activity, which may in turn protect against hypertension.342 In vascular ECs, IgG released from B cell binding to Fcγ receptors (FcγRs) and inhibiting the activity of eNOS synthase, which contributing to obesity-induced hypertension.343. Here, PTGS2 is linked to hypertensive disorder.